The specificity of Helicobacter pylori for the human host is the consequence of a series of adaptations that probably occurred many thousands of years ago. This adaptation has provided H. pylori with an important advantage in vivo because unlike most gastrointestinal pathogens, it has little competition from other bacteria in its preferred ecological niche. One consequence of the high degree of host adaptation of H. pylori is that it cannot survive for long periods outside the body. H. pylori has evolved several mechanisms that enable it to vary gene expression and that are critical for host adaptation. Although clinical studies provide the most accurate means of studying H. pylori adaptation to the host, such studies suffer from obvious limitations. The availability of small animal models of H. pylori infection has permitted an improved understanding of H. pylori adaptation to the host. Much of our current understanding of H. pylori pathogenesis has been derived from in vitro studies. Nevertheless, in vitro methods cannot reproduce the complex interactions between pathogen and host. An important aspect of such interactions that is absent from in vitro assays is the host's immune response. Metabolic functions are likely to play an important role in H. pylori colonization of, and adaptation to, the host. This observation would be consistent with the findings from in vivo-based investigations of bacterial virulence in other pathogens. Colonization of animal hosts by H. pylori isolates have been discussed in this chapter.

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